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Lipid droplets（LD）are storage organelles that consist of a core of neutral lipids and sur-rounded by phospholipid monolayer.Lipid droplets play a key role in energy,lipid home-ostasis and the normal function of cells and organelles.Endoplasmic reticulum（ER）is engaged in certain activities such as the synthesis of lipids,cholesterol and proteins.Previous studies have shown that misfolded or unfolded protein accumulation can induce damage to ER,ultimately inducing ER stress and the unfolded protein response（UPR）.Recent studies showed that besides protein accumulation,deregulation of lipid droplets metabolism can also result in ER stress and UPR activation.Inositol-requiring enzyme 1（IRE1）is the most conserved transducer of UPR.The activation of IRE1 not only can splice the transcription factor XBP1 but also can target a group of m RNAs and micro RNAs for degradation through a process known as regulated IRE1dependent decay（RIDD）.In 2006,Hollien and Weissmann discovered RIDD in Drosophila and later studies have shown that RIDD can control cell fate.One of the targets of RIDD is the Drosophila fatty-acid transport protein（d FATP）,which is central player in lipid metabolism.It has been shown that d Fatp is sufficient for the size expansion of lipid droplets in retinal pigment cells.Besides,lipid droplets in retinal pigment cells are required for photoreceptor survival during aging.In Drosophila,retinal pigment and photoreceptor cells both belongs to the Drosophila central nervous system（CNS）,which consists of the ventral nerve cord,central brain,retina and the optic lobe.This thesis aims to study the role of RIDD（ire1/d Fatp）on lipid droplets metabolism in the young adult Drosophila retina in physiological and pathological conditions.Here,we found that it is ire1 but not xbp1 that can inhibit d Fatp and the subsequent d Fatp-dependent lipid droplet accumulation in retinal pigment cells.These results suggest an ire1-dependent,possibly RIDD-dependent inhibition of d Fatp in retinal pigment cells.In Drosophila retina,the misfolding rhodopsin-1（rh1）mutation(nina EG69D,termed rh1G69Dfor clarity)induces chronic ER stress in photoreceptor cells and activation of ire1/xbp1.In addition,nina A is a gene that encodes chaperone,which is specific for the folding of rh1.Nina AE110Vmutation can lead to mild ER stress in photoreceptor cells and also activate ire1/xbp1.Therefore,nina AE110V,rh1G69Dand 54C-gal4＞UAS-rh1G69D(which uses 54C driver to express rh1G69Dmutant in retinal pigment cells)are three pathological conditions to induce ER stress in the young adult Drosophila retina.We observed a complete suppression of d Fatp expression and lipid droplets clearance in retinal pigment cells of nina AE110Vmutant flies.However,there is a lot of lipid droplet accumulation in both rh1G69Dand 54C-gal4＞UAS-rh1G69Dmutant in young adult Drosophila retina.This may be due to the fact that there is a stronger RIDD activation in nina AE110Vmutation than in rh1G69Dand 54C-gal4＞UAS-rh1G69Dmutations,and RIDD leads to more decay of d Fatp,resulting in lipid droplets clearance in nina AE110V.Another model of lipid droplets accumulation of retinal pigment cells is mutations in aats-met,a gene of the mitochondrial respiratory complex.In this thesis,we found that nina AE110Vmutation can suppress the abnormal lipid droplets accumulation in aats-met mutation.The experimental results reveal that a depletion of d FATP in photoreceptor presumably due to ire1 activation in nina A mutant can lead to lipid droplets clearance in aats-met mutant.This thesis also investigates whether mutation in d Wdr45,the Drosophila orthologue of Wdr45,which causesβ-propeller associated neurodegeneration（BPAN）in humans,is a good model to study ER stress and the regulation of lipid metabolism.In this thesis,d Wdr45knockdown was used to investigate neurodegeneration and lipid droplet accumulation in the young adult Drosophila retina.Here we report that,there is lipid droplet accumulation accompanied by degeneration of photoreceptors in BPAN.